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An integrated and projected‐based laboratory course was described, integrating interconnected knowledge points and biochemistry and molecular biology techniques on a research project‐based system. The program, which served as an essential extension of theoretical courses to practice, was conducted with a sophomore of basic medical science who had completed the course in medical biochemistry and molecular biology. This course engaged students in learning "genetic manipulation" and "recombinant DNA technology" to understand the target gene's role in disease mechanics, thus altering evaluation and treatment for clinical disease. Students could master applied and advanced techniques, such as cell culture, transfection, inducing exogenous fusion protein expression, purifying protein and its concentration assay, quantitative polymerase chain reaction, and western bot analysis. This laboratory exercise links laboratory practices with the methods of current basic research. Students need to complete the experimental design report and laboratory report, which could be advantageous for improving their ability to write lab summaries and scientific papers in the future. The reliability and validity analyses were conducted on the questionnaire, and we examined students' satisfaction with the course and their gains from the course. The student feedback was generally positive, indicating that the exercise helped consolidate theoretical knowledge, increase scientific research enthusiasm, and provide a powerful tool to be a better person and make informed decisions. [ABSTRACT FROM AUTHOR]

Lung adenocarcinoma (LUAD) is a serious threat to public health and is accompanied by increased morbidity and mortality worldwide. Neuronal PAS domain protein2 (NPAS2) has been confirmed as an oncogene in LUAD; however, little is known about its molecular mechanism. Here, the expression level of NPAS2 was detected in LUAD cell lines and 16HBE cells. Gain‐ and loss‐of‐function experiments were performed. Cell Counting Kit‐8, colony formation, flow cytometry, wound‐healing and Transwell assays were conducted to assess cell proliferation, apoptosis, migration and invasion, respectively. Reprogramming of glucose metabolism was evaluated via oxygen consumption rate (OCR), complexes activities, lactic production and glucose consumption. The expression of critical proteins was examined by western blot. We demonstrated aberrant upregulation of NPAS2 and β‐arrestin‐1 (ARRB1) in LUAD cell lines. ARRB1 was found to be a critical transcription factor of NPAS2 with binding sites within the promoter region of NPAS2, thereby causing its transcriptional activation. Functional experiments revealed that NPAS2 depletion significantly inhibited the malignant behaviours of A549 cells by suppressing cell proliferation, migration, invasion and epithelial‐mesenchymal transition and promoting cell apoptosis. Meanwhile, NPAS2 depletion increased OCR and activities of complexes (I, II, III and V), and reduced lactic acid production and glucose uptake in A549 cells, indicating that NPAS2 depletion inhibited aerobic glycolysis, accompanied by reduced expression of glycolytic enzymes. However, the changes caused by NPAS2 knockdown were partly restored by ARRB1 overexpression. In conclusion, our study suggests that ARRB1 could transcriptionally activate NPAS2, facilitating malignant activities and glycolysis, and ultimately promoting the progression of LUAD, proving a novel therapeutic strategy for the treatment of LUAD. [ABSTRACT FROM AUTHOR]

Due to the "shuttle effect" and low conversion kinetics of polysulfides, the cycle stability of lithium sulfur (Li−S) battery is unsatisfactory, which hinders its practical application. The Mott‐Schottky heterostructures for Li−S batteries not only provide more catalytic/adsorption active sites, but also facilitate electrons transport by a built‐in electric field, which are both beneficial for polysulfides conversion and long‐term cycle stability. Here, MXene@WS2 heterostructure was constructed by in‐situ hydrothermal growth for separator modification. In‐depth ultraviolet photoelectron spectroscopy and ultraviolet visible diffuse reflectance spectroscopy analysis reveals that there is an energy band difference between MXene and WS2, confirming the heterostructure nature of MXene@WS2. DFT calculations indicate that the Mott‐Schottky MXene@WS2 heterostructure can effectively promote electron transfer, improve the multi‐step cathodic reaction kinetics, and further enhance polysulfides conversion. The built‐in electric field of the heterostructure plays an important role in reducing the energy barrier of polysulfides conversion. Thermodynamic studies reveal the best stability of MXene@WS2 during polysulfides adsorption. As a result, the Li−S battery with MXene@WS2 modified separator exhibits high specific capacity (1613.7 mAh g−1 at 0.1 C) and excellent cycling stability (2000 cycles with 0.0286 % decay per cycle at 2 C). Even at a high sulfur loading of 6.3 mg cm−2, the specific capacity could be retained by 60.0 % after 240 cycles at 0.3 C. This work provides deep structural and thermodynamic insights into MXene@WS2 heterostructure and its promising prospect of application in high performance Li−S batteries. [ABSTRACT FROM AUTHOR]

Background and Objectives: Hepatitis E virus (HEV) is an underrecognized and emerging infectious disease that may threaten the safety of donor blood supply in many parts of the world. We sought to elucidate whether our local community blood supply is at increased susceptibility for transmission of transfusion‐associated HEV infections. Materials and Methods: We screened 10,002 randomly selected donations over an 8‐month period between 2017 and 2018 at the Stanford Blood Center for markers of HEV infection using commercial IgM/IgG serological tests and reverse transcriptase quantitative polymerase chain reaction assays (RT‐qPCR). Donor demographic information, including gender, age, self‐identified ethnicity, location of residence and recent travel, were obtained from the donor database and used to generate multivariate binary logistic regressions for risk factors of IgG seropositivity. Results: A total of 10,002 blood donations from 7507 unique donors were screened, and there was no detectable HEV RNA by RT‐qPCR. The overall seropositivity rate was 12.1% for IgG and 0.56% for IgM. Multivariate analysis of unique donors revealed a significantly higher risk of IgG seropositivity with increasing age, White/Asian ethnicities and residence in certain local counties. Conclusion: Although HEV IgG seroprevalence in the San Francisco Bay Area is consistent with ongoing infection, the screening of a large donor population did not identify any viraemic blood donors. While HEV is an underrecognized and emerging infection in other regions, there is no evidence to support routine blood screening for HEV in our local blood supply currently; however, periodic monitoring may still be required to assess the ongoing risk. [ABSTRACT FROM AUTHOR]

Background & Aims: Human neutrophil peptides (HNP)‐1, ‐2 and ‐3 are the most abundant proteins in neutrophil azurophilic granules and are rapidly released via neutrophil degranulation upon activation. The aims of our study were to assess the role of HNP1‐3 as biomarkers of disease severity in patients with decompensated cirrhosis and their value in predicting short‐term mortality. Methods: In this study, 451 patients with acutely decompensated cirrhosis (AD) were enrolled at the two medical centres. Overall, 281 patients were enrolled as the training cohort from October 2015 to April 2019, and 170 patients were enrolled as the validation cohort from June 2020 to February 2021. Plasma HNP1‐3 levels were measured using enzyme‐linked immunosorbent assay (ELISA). Results: Plasma HNP1‐3 increased stepwise with disease severity (compensated cirrhosis: 0.3 (0.2–0.4); AD without acute‐on‐chronic liver failure (ACLF): 1.9 (1.3–4.8); ACLF‐1: 2.3 (1.8–6.1); ACLF‐2: 5.6 (2.9–12.3); ACLF‐3: 10.3 (5.7–17.2) ng/ml). From the multivariate Cox regression analysis, HNP1‐3 emerged as independent predictors of mortality at 30 and 90 days. Similar results were observed in the subgroup analysis. On ROC analysis, plasma HNP1‐3 showed better predictive accuracy for 30‐ and 90‐day mortality (area under the receiver operating characteristic (AUROC) of 0.850 and 0.885, respectively) than the neutrophil‐to‐lymphocyte ratio (NLR) and similar accuracy as end‐stage liver disease (MELD: 0.881 and 0.874) and chronic liver failure‐sequential organ failure (CLIF‐SOFA: 0.887 and 0.878). Conclusions: Plasma HNP1‐3 levels were closely associated with disease severity and might be used to identify patients with AD at high risk of short‐term mortality. [ABSTRACT FROM AUTHOR]

Objective: To investigate the underlying causes of false positives in NIPT of fetal sex chromosomal aneuploidies using fetal cell‐free DNA from maternal plasma. Methods: In the present study, we focus on a cohort of 23,984 pregnancy cases with NIPT. Karyotyping and FISH analysis were employed to verify the NIPT detected false‐positive results of fetal sex chromosomal aneuploidies, and a comparative CNV sequencing on positive and negative NIPT cases was uniquely performed to elucidate the underlying causes. Results: A total of 166 cases (0.69%) were identified as fetal sex chromosomal abnormalities, while 84 cases were found to be false‐positive results possibly associated with maternal X chromosomal aneuploidies (n = 8), maternal X chromosomal structural abnormalities (n = 1), maternal CNVs (n = 4) as well as known placental mosaicism (n = 1). Furthermore, our study showed that the maternal chromosome CNV between 1–1.6 Mb was associated with false‐positive NIPT results in sex chromosomal abnormalities. Conclusion: Our research demonstrated the spectrum of factors causing false positives in NIPT of fetal sex chromosomal abnormalities based on a large cohort. The effective maternal CNV size cut‐off identified in our study could integrate into bioinformatics algorithms for reducing the false‐positive rate, however, further investigation is necessary to confirm this. [ABSTRACT FROM AUTHOR]

The COVID‐19 pandemic is a huge challenge to education systems. Most governments around the world have temporarily closed schools, universities, and colleges. At the same time, teachers and students are encouraged to use the online and distance learning programs and platforms as an alternative. In the present study, we proposed a series of innovative solutions in Medical Molecular Biology education during the COVID‐19 pandemic in China, including a flipped classroom model, live streaming course, chat Apps, and scientific papers on COVID‐19 as additional learning material. Our results demonstrated that these innovations not only help teachers to maintain the teaching process as usual but also be useful for protecting students from psychological trauma. Our study indicates that online education with a well‐designed workflow for conducting provides an alternative approach for teachers to maintain quality education during the onset of the emerging crisis. [ABSTRACT FROM AUTHOR]

Ischemia/reperfusion (I/R) is a well‐known injury to the myocardium, but the mechanism involved remains elusive. In addition to the well‐accepted apoptosis theory, autophagy was recently found to be involved in the process, exerting a dual role as protection in ischemia and detriment in reperfusion. Activation of autophagy is mediated by mitochondrial permeability transition pore (MPTP) opening during reperfusion. In our previous study, we showed that MPTP opening is regulated by VDAC1, a channel protein located in the outer membrane of mitochondria. Thus, upregulation of VDAC1 expression is a possible trigger to cardiomyocyte autophagy via an unclear pathway. Here, we established an anoxia/reoxygenation (A/R) model in vitro to simulate the I/R process in vivo. At the end of A/R treatment, VDAC1, Beclin 1, and LC3‐II/I were upregulated, and autophagic vacuoles were increased in cardiomyocytes, which showed a connection of VDAC1 and autophagy development. These variations also led to ROS burst, mitochondrial dysfunction, and aggravated apoptosis. Knockdown of VDAC1 by RNAi could alleviate the above‐mentioned cellular damages. Additionally, the expression of PINK1 and Parkin was enhanced after A/R injury. Furthermore, Parkin was recruited to mitochondria from the cytosol, which suggested that the PINK1/Parkin autophagic pathway was activated during A/R. Nevertheless, the PINK1/Parkin pathway was effectively inhibited when VDAC1 was knocked‐down. Taken together, the A/R‐induced cardiomyocyte injury was mediated by VDAC1 upregulation, which led to cell autophagy via the PINK1/Parkin pathway, and finally aggravated apoptosis. [ABSTRACT FROM AUTHOR]

The rapid development and popularization of smart phones and mobile internet has created a new social lifestyle, and correspondingly prompts the transformation of network teaching from desktop computer to mobile teaching. This article has compared the pros and cons of Tsinghua Education Online and WeChat official account (WOA) in fulfilling teaching functions. We also described the construction of WOA platform with the example of WOA‐based teaching in biochemistry and molecular biology. The platform can establish nearly 75 menu catalogs and 2,250 items, which is capable for the publication of any types of teaching materials and information. The WOA teaching is well accepted and becomes popular in China due to the free, interactive, attractive, adaptable, portable, sustainable, and more participatory teaching styles. © 2018 International Union of Biochemistry and Molecular Biology, 46(5):555–560, 2018. [ABSTRACT FROM AUTHOR]